Abstract
Electrical injury can cause a variety of cardiac arrhythmias. Atrial fibrillation as a result of such injury is fairly rare, however, and is rarer still in cases of low-tension electrical injury. We present the case of a patient who developed acute atrial fibrillation in association with low-voltage electrical injury, which resolved after the intravenous administration of digoxin.
Key words: Accidents, occupational; atrial fibrillation/etiology; electric injuries/complications
Electrical injury can cause various cardiac dysrhythmias such as asystole, ventricular fibrillation, sinus tachycardia, and heart blocks. However, supraventricular tachyarrhythmias, such as atrial fibrillation, are rare.1–7 The patient in the present case had acute atrial fibrillation that developed from low-voltage electrical injury and resolved after the intravenous administration of digoxin.
Case Report
In May 2003, a 42-year-old worker experienced a low-tension (<350 V) electrical injury as a consequence of an occupational accident. He lost consciousness for a few minutes and was referred to the emergency department of our hospital. He had palpitations on admission. On physical examination, the arterial blood pressure was 130/70 mmHg, and the heart rate was 144 beats/min and irregularly irregular. There was a small superficial entrance wound on the right hand. Auscultation revealed tachyarrhythmia (irregularly irregular sounds) but no cardiac murmur. Electrocardiography showed acute atrial fibrillation (AF) with rapid ventricular response (Fig. 1). A careful interview of the patient revealed that no episode of palpitation had occurred before the electrical accident. Intravenous digoxin was given to decrease the heart rate. The AF converted to sinus rhythm in 1 hour (Fig. 2). After 24-hour cardiac monitoring in the emergency department with continuous telemetry and serial electrocardiograms, no cardiac arrhythmia was detected and he was sent home.

Fig. 1 An electrocardiogram at admission shows atrial fibrillation.

Fig. 2 An electrocardiogram 1 hour after admission shows sinus rhythm.
Subsequently, the patient was asked to appear at our outpatient clinic for further investigation of the AF. The results of routine laboratory tests, including tests of thyroid function, were within normal ranges. Follow-up electrocardiography showed normal sinus rhythm. Echocardiography revealed normal left ventricular size and function and no valvular disease. Exercise stress testing was negative. Holter monitoring showed rare ventricular premature beats, with no episode of AF.
Discussion
Atrial fibrillation can occur in both cardiac and noncardiac disease or it can appear in the absence of any overt condition. Common causes include hypertension, valvular disease, coronary heart disease, cardiac surgery, thyrotoxicosis, excessive consumption of alcohol, and cardiomyopathy.
The heart is one of the organs most vulnerable to electrical injury. Electrical injury may cause direct necrosis of the myocardium or cardiac dysrhythmia. Asystole and ventricular fibrillation are the most serious of the cardiac complications of electrical injury. Other possible rhythm disturbances include sinus tachycardia, bradycardia, and nonspecific ST-T wave changes; then there are conduction defects such as various degrees of heart block, prolongation of the QT interval, and bundle brunch block.1 Supraventricular tachycardia and sick sinus syndrome have been reported.2 The association of atrial fibrillation with electrical injury is rare3–7 and has usually occurred in instances of high-tension (>1,000 V) electrical shock. Atrial fibrillation as a result of low-tension electrical injury has, however, been reported.3 We add to the literature this report of a 42-year-old man who experienced transient atrial fibrillation as a result of low-tension electrical injury.
Cardiac dysrhythmias are more frequent in patients who lose consciousness at the time of injury and in patients who experience a high-tension electrical injury.8 Exposure to high-tension current will most likely cause ventricular asystole. The pathogenesis of the other cardiac dysrhythmias is rather unclear and is most likely multifactorial. Possible mechanisms include arrhythmogenic foci due to myocardial necrosis, alterations in the Na+- K+-adenosine triphosphatase concentration, and changes in the permeability of myocyte membranes. Last, cardiac injury and rhythm disturbances can be caused by anoxic injury in cases in which respiratory arrest precedes the injury to the heart.9
The need for cardiac monitoring after electrical injury is less well defined. The criteria for cardiac monitoring after an electrical injury are these: loss of consciousness, abnormal electrocardiogram on admission, exposure to high voltage, and a history of cardiac disease (especially a history of cardiac arrhythmia).9 Our patient had lost consciousness and had manifested atrial fibrillation at admission. Therefore, we ordered 24-hour cardiac monitoring with continuous telemetry and serial electrocardiograms, and we detected no rhythm disturbances.
In conclusion, low-tension electrical injury can infrequently cause atrial fibrillation. This is usually a benign condition that is likely to revert to sinus rhythm spontaneously.
Footnotes
Address for reprints: Ercan Varol, MD, Anadolu Mah., ESO (Memur) evleri, C Blok, No:5, 32200 Isparta, Turkey
E-mail: mehmetozaydin@hotmail.com
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